2. 8
STEPS TO OPTIMIZING PREOPERATIVE OUTCOMES
a. Assess
patients clinical findings
b. Evaluation
of functional status
c. Consider
the patient’s surgery specific risks
d. Decide
if further non-invasive evaluation is needed
e. Decide
when to recommend invasive evaluations
f. Optimize
medical therapy
g. Perform
appropriate preoperative surveillance
h. Design
maximal long-term therapy
3. ASSESSING
CLINICAL FEATURES (STEP 1)
a. H
& P
b. High
risk status includes:
ii. Decompensated
heart failure
iii. Unstable
angina
iv. Symptomatic
arrhythmias
v. Symptomatic
valvualr disease
c. Stable
conditions that are affected with surgical stress.
i. Stable
angina
ii. Distant
MI
iii. Prior
HF
iv. Moderate
valve disease
d. Identify
serious co-morbidity
i. Diabetes
ii. Stroke
iii. Renal
insufficiency
iv. Pulmonary
disease
4. EVALUATING
FUNCTIONAL STATUS (STEP 2)
a. Assess
functional capacity
i. Exercise
tolerance
ii. MET
– Metabolic Equivolence Test (activity level)
iii.
5. SURGERY-SPECIFIC
RISK FACTORS (STEP 3)
a. High
risk (reported cardiac risk* ≥5%)
b. Emergency
major operations, particularly in the elderly
c. Aortic,
major vascular, and peripheral vascular surgery
e. Intermediate
risk (reported cardiac risk ≥1%, <5% )
f. Intraperitoneal
and intrathoracic
g. Carotid
endarterectomy
h. Head
and neck surgery
i. Orthopedic
surgery
j. Prostate
surgery
k. Low
risk (reported cardiac risk <1%)
l. Endoscopic
procedures
m. Superficial
biopsy
n. Cataract
surgery
o. Breast
surgery
6. PREOPERATIVE
INVASIVE VS. NON-INVASIVE TESTING (STEP 4)
a. Patients
at low risks with steps 1-3 generally do not require additional evaluation.
b. High
risk patients may benefit
c. Patients
with more than 3 clinical risk factors and extensive myocardial ischemia on
preop stress test may have a high risk of complications, and require beta
therapy or invasive evaluation[WU4] .
d. EKG
EVALUATION
i. Greater
than 1mm ST segment elevation in standard leads, and 2mm elevation in precordial
leads.
ii. T
wave inversion in leads I, II, V3-V6.
iii. Lead
II
v. Preop:
1. ST
segment represents phase II of the cardiac action potential (slow
repolarization)
2. Signs
of ischemia
a. II,
III, Avf = Right coronary
b. I,
Avr = circumflex
c. V3-V5
= L anterior descending
3. Arrhythmias
4. Electrolyte
disturbances
5. Hypertrophy
vi. EKG-
ST segment >1mm during angina confirms an MI.
e. EXERCISE
STRESS TEST
i. Used
to evaluate ventricular function and prognosis.
ii. Some
conditions do not permit an EST.
1. PVD
2. Pacemakers
3. Severe
aortic stenosis
4. Lung
disease
iii. Criteria
for abnormalities:
1. 1mm
ST segment elevation or depression within 4 minutes of exercising.
2. The
prognosis is poor if the ST segment abnormality is associated with angina, or a
decrease in systolic blood pressure[WU7] .
3. More
cost effective.
f. NON-INVASIVE
IMAGES
ii. The
heart is induced with adenosine or persantine in order to produce vasodilation,
or doputamine to raise the heart rate to exercise levels
iii. The
patient is monitored for a change in EKG, and a radionucleotide tracer is placed to check for myocardial
function.
iv. ECHOCARDIOGRAM
1. Wall
stress is elevated after stressing the heart with dobutamine or pacing.
2. Contrast
dye can be given to enhance the images.
v. TRANS-ESOPHAGEAL
ECHO
1. TEE
is 2 dimensional tool used to measure contractility.
2. Able
to see ventricular as well as valve activity in real time
3. Uses:
a. Measuring
stenotic and regurgitant lesions
b. Hypokinesis,
dyskinesis, or akinesis
c. Contractility
d. Volume
status
e. Ventricular
dysfunction
4. Gold
standard for eval of cardiac patient; preferred over PAC intraop
g. INVASIVE
MONITORING (STEP 5) - CATH
i. Indicated
when:
1. Presence
of residual ischemia after MI
2. Unstable
angina
ii. Stent
placement prior to surgery
1. Risks
of thrombosis and bleeding post-op.
iii. AHA/ACC
recommends waiting at least 2-4 weeks after stent for non-cardiac surgery
7. OPTIMIZING
THERAPY (STEP 6)
a. Most
patients with a history of angina will be on beta blockers, calcium channel
blockers, aspirin
c. Heart
failure patients may be on ACE inhibitors, and beta blockers.
d. Smokers-
are encourage to stop smoking.
8. PREOPERATIVE
SURVEILLANCE (STEP 7)
a. EKG-
base line, immediately after surgery and 2 days post-op.
b. Bio
markers such as CK MB maybe elevated immediately post-op. Watch for increases
in those numbers.
c. New
EKG abnormalities.
d. Patients
who develop ST segment changes should be considered for cardiac
catheterization.
9. MAXIMAL
LONG-TERM THERAPY (STEP 8)
a. Evaluation
before and after non-cardiac surgery can be used to optimize a patients
condition, and modify the risks.
b. Patients
with history of repetitive post-op complications are at greater risk for long
standing issue.
10. ANESTHETIC
MANAGEMENT OF MYOCARDIAL INFARCTION AND HYPERTENSION
11. CORONARY
ARTERY DISEASE
a. Affects
an estimated 10 million people in the US
b. 5-10%
of the patients undergoing anesthesia
have heart disease.
c. Careful
evaluation of the patient can help reduce the M&M associated with cardiac
patients undergoing non-cardiac surgery.
12. PREOPERATIVE
ASSESSMENT
a. Determine
the severity, progression and functional limitations.
b. Determine
if the are in high risk or low risk group.
c. If
a patient can climb three flights of steps they are considered to have good
conditioning.
13. COMPLICATIONS
ASSOCIATED WITH MI
a. Arrythmias
b. Pericarditis
c. Mitral regirgitation
d. Ventricular Septal rupture
e. Congestive Heart
f. ARRYTHMIAS
i. Are
common complications post MI
ii. V-fib
1. Occurs
in 3-5% of the population.
2. Usually
occurs within the first 4hrs
3. Rx:
Rapid defibrillation 200-300j
a. Lidocaine
1-1.5 mg/kg
b. Amiodarone 300 mg in 20-30cc D5W loading (arrest), 150 mg in a 100cc bag
of D5W given over 10 minutes (Loading infusion), 360 mg over 6H.
c. Beta
Blockers decreases incidence of V-fib very early on.
1. Rx.
Symptomatic V-tach with defibrillation
2. Asymptomatic
V-tach with Lidociane
iv. A-fib
1. Most
common artial arrythmia
2. Occurs
in 10% of the population
3. Rx:
Symptomatic is Rx with Cardioversion
4. asymptomatic
with B-blockers, Ca channel blockers
v. Brady-dysrrthmias.
1. Common
post IWMI (inferior wall MI)
2. May
reflect parasympathetic activity or acute ischemia of the SA or AV node.
3. Rx:
a. Atropine
or pacer if needed.
b. 2nd
and 3rd degree heart block occurs in approximately 30% of IWMI.
g. PERICARDITIS
i. A
common complication of acute MI and can be confused with angina.
ii. Unlike
angina pericarditis will pain will change with changes in position, and upon
taking a deep breath.
iii. Pericardial
friction rub may be present.
iv. May
see diffuse ST or T wave changes.
1. Rx;
aimed at relief of chest pain
2. ASA,
indomethacin and corticosteroids.
v. Dressler’s
syndrome: Is a delayed form of pericarditis that occurs weeks to several months
after an MI.
h. MITRAL
REGURGITATION
ii. Severe MR occurs 10 times more likely post
IWMI.
iii. Severe
acute MR results in pulmonary edema and heart failure.
iv. Total
papillary muscles rupture results in death within 24 hours.
v. Rx:
Decrease afterload, Nipride, or balloon pump until surgery.
i. VENTRICULAR
SEPTAL RUPTURE
i. Mortality
rate is 20%
ii. Requires
emergency surgery if hemodynamically unstable.
iii. Seen
with AWMI
iv. Dx:
holosystolic murmur
v. Place
on balloon pump as soon as diagnosed.
j. CONGESTIVE
HEART FAILURE AND CARDIOGENIC SHOCK
i. Most
acute MI patients will have some degree of heart failure.
ii. Cardiogenic
shock: is an advanced form of heart failure in which cardiac out put is not
sufficient to maintain perfusion of vital organs.
iii. Cardiogenic
shock is seen in 40% of left ventricular MI.
iv. Rx:
v. Norepinephrine
(4mg/1000cc D5W)- 2-4mcg/min
1. α¹
& α²
vi. Vasopressin-
0.01-0.04 U/min
vii. Dopamine-
0.5-2.0mcg/kg/min (Dopa)
1. 2-10mcg/kg/mi
(Dopa/Beta)
2. 10-20mcg/kg/min
(Alpha)
viii. Dobutamine-2.5-15mcg/kg/min
1. Beta
1 agonist
ix. If
Bp is stable administration of nitro can be given to decrease LV preload and
after load.
14. RIGHT
VENTRICULAR INFARCTION
a. Occurs
in about 1/3rd of patients with acute inferior wall left ventricular
MI
b. An
isolated acute inferior wall MI to the right ventricle is very unusual.
c. Dx:
i. clinical
triad; hypotension, jugular venous distention and clear lung fields. Kussmaul’s
sign (JVD with inspiration) can be seen.
d. 1/3rd
of patients with right ventricular MI will develop A-fib.
e. 50%
of the patients' may develop H.B
f. Dx:
i. Recognition
of right v.s left ventricular MI.
2. ST
elevation >1mm on V4 right, St elevation >1mm on V1.
ii. Treatment
of left ventricular MI in the face of right ventricular MI can worsen the
condition.
iii. Diuretics
and vasodilators are undesirable.
g. RX:
i. Av
sequential pacing
ii. Restore
intravascular volume
iii. Administration
of positive inotrope.
iv.
15. CEREBRAL
VASCULAR ACCIDENT (CVA)
a. May
be seen most commonly after an MI of the anterior wall and the apex of the left
ventricle.
b. Thrombus
formation can be seen in 1/3rd of the patients.
c. DX:
Echo
d. RX:
Anticoagulants
16. INTRAOPERATIVE
MANAGEMENT OF PT WITH ISCHEMIC HEART DISEASE: Induction, Maintenance, Emergence
a. GOAL
OF ANESTHETIC MANAGEMENT
i. Goal
is to prevent ischemia by:
1. Increasing
myocardial O2 supply
2. Decrease
myocardial O2 demand
3. Monitor
arrythmias and treatment if it develops
ii. Events
that increase risks are:
2. Standard
is to keep HR and BP at 20% of baseline.
b. INTRAOPERATIVE
EVENTS THAT EFFECT O2 SUPPLY/DEMAND
i. Increased
O2 requirements
1. Increased SNS
2. Tachycardia
3. Hypertension
4. Increased
contractility
5. Increased
after load
ii. Decreased
O2 delivery
1. Tachycardia
2. Diastolic
hypotension
3. Hypocapnea
4. Decreased
O2
c. ANESTHETIC
INDUCTION IN THE PRESENCE OF PREVIOUS MI
ii. MR
facilitates intubation
iii. Keep
intubations at no greater than 15secs.
iv. Fentanyl
1-3mcg/kg
v. Nitro
0.25-1.0mcg/kg/min
vi. Laryngeal
tracheal lidocaine (LTA)
d. PHYSIOLOGIC
RESPONSES DURING INDUCTION
i. Tachycardia:
Hr > 110
ii. Hypertension:
1. Nipride
– 1-2mcg/kg 15s before DL
2. Nitroglycerin
(better choice for MI with normal BP) 10-20mcg/min
iii. Hypotension:
e. MAINTENANCE
i. Normal
LV function
1. Inhalationals
are acceptable for Rx of HTN.
2. Opioid/fentanyl
technique + inhalationals
1. Use
short acting opioids over volatile anesthetics
2. With
severe disease you can use high dose opioids + nitrous
3. Consider
regional technique
4. Select
MR with limited CV effects
f. CHOICES
OF MUSCLE RELAXANT
i. Chose
MR with limited side effects
1. Vec
2. Roc
3. Cis
ii. Histamine
release MR
1. Atracurium
à
avoid
iii. Increase
in HR
1. Pancuronium
iv. Reversals
g. SHIVERING
AFFECTS ON THE HEART
i. Increases
myocardial O2 demand- 500%
ii. Loss
of body temperature in the OR is common, and in the post op period.
iii. Ways
to increase body temp:
1. Warmed
fluids
2. Inspired
O2
3. Warming
blanket
17. MANAGEMENT
OF PT WITH ESSENTIAL HYPERTENSION
a. PREOPERATIVE
EVAL
i. Goal:
1. Aimed
at determining adequacy of blood pressure control, and hypertensive drug
therapy.
2. Drug
therapy should continue preoperatively and should continue in the perioperative
period.
3. There
is no evidence of postop complications increasing in the patient with
hypertension, however, preop HTN may increase incidence of postop MI.
ii. If
a hypertensive patients exhibit signs of end organ damage then elective surgery
needs to be post-poned.
iii. White
coat syndrome
iv. Evaluate
end organ damage; heart failure, LV hypertrophy, CVA etc.
v. Evaluate
drug therapy: Many antihypertensive drugs will affect the autonomic nervous
system. This will manifest it’s self as orthostatic hypotension.
vi. Rebound
hypertension may occur with certain drugs such as Beta blockers, and clonidine.
vii. During
anesthesia you may see exaggerated responses to blood loss, positive pressure
ventilation or sudden changes in body position.
b. INDUCTION
OF ANESTHESIA
i. Rapid
acting intravenous agents- can cause a dramatic decrease in Bp due to
peripheral vasodilation and decreased intravascular volume. (propofol)
ii. Intubation
iii. Keep
DL < 15sec.
c. MAINTENANCE
OF ANESTHESIA WITH HTN
i. Volatile
anesthetics and nitrous allows for rapid changes in depth in response to
changes in BP.
ii. Opioids
and nitrous
v. Treat
the underlying cause.
1. Volume=
replace with volume.
2. Anesthetic
depth=increase anesthesia
d. MONITORS
i. Depends
on the type of surgery
1. EKG
ii. Regional
anesthesia
1. Take
caution for hypotension
e. POSTOPERATIVE
MANAGEMENT
i. Episodes
of hypertension are common postop.
ii. Treat
with peripheral vasodilators
1. Hydralizine
5-10mg Q 10-20 minutes
2. Labetolol
0.1-0.5mg/kg
3. Nipride
infusion- 0.5-8mcg/kg/min, not to exceed 10mcg/kg/min for more than 10 minutes.
19. DISORDERS
OF THE CONDUCTION SYSTEM
a. Review
of EKG
b. What
are the basic areas to look at on EKG?
i. HR-
60-80
ii. P
waves- Atrial depolarization. Up right in lead II, III, AVF
iii. PR
interval- represents electrical signal from SA-AV node. Normally 0.12-20s
iv. QRS
complex- Ventricular depolarization. Normal 0.04-0.12
v. Ventricular
rate
vi. Any
early beats, pauses after the QRS
c. CLASSIFICATION
OF CONDUCTION ABNORMALITIES
i. Are
classified based on where the block is located in respect to the AV node.
ii. Blockage
above the AV node- are usually benign and transient.
iii. Blockage
below the AV node- tend to be progressive and permanent.
d. HEART
BLOCK
i. What
is heart block?
1. Impairment
of the conduction system in sending signals from the SA-AV node.
ii. What
are the types of heart block?
1. First
degree
2. Second
degree
3. Third
degree
4. RBBB
5. LBBB
e. CLASSIFICATION
OF HEART BLOCK
1. First
degree heart block.
a. Electrical
impulses move slowly from the SA to the AV node.
b. EKG
shows a PR interval of > 0.20sec, HR and the heart itself is normal.
2. Seen
in:
a. Patients
on digoxin, healthy athletes
3. Treatment?
a. None
b. Treatment
of first degree heart block is usually not an issue in anesthesia.
c. Monitoring
of the condition to make sure it doesn’t
progress to second degree type I.
iii. SECOND
DEGREE
1. SECOND
DEGREE TYPE 1 (WENCKEBACH)
a. Second
degree type I (Mobitz type I)
b. Some
signals don’t reach the ventricle dropping some beats.
c. Wenckebach
i. Electrical
signals are delayed more and more with each beat until one beat is skipped.
d. The
conducted beat will have a short PR interval.
e. S/S
i. usually
dizziness
f. Seen
in:
i. Patients
with an inferior wall MI.
ii. Self
limiting, and usually doesn’t require treatment.
3. SECOND
DEGREE TYPE 2
a. Mobitz
type II
i. less
common, but more serious.
ii. The
electrical signal cannot reach the ventricle and the patient may have an
abnormally slow HR.
iii. Excitation
intermittently fails to pass through the AV node, or Bundle of His.
iv. THIRD
DEGREE
1. The
hearts electrical signal doesn’t pass from the SA to the AV node (AV node
dissociation).
2. Independent
ventricular pacemaker takes place.
3. There
is no relationship between the p waves and QRS.
4. The
heart contracts but with less force.
5. Seen
in:
a. Pt’s
with heart disease
b. Drug
toxicity- digoxin
c. Congenital
d. Post
MI
f. Surgical
stimulation
g. Stop,
give atropine. Or glyco
6.
TREATMENT
OF THIRD DEGREE
b. Isoproteranol:
Potent B1, B2 agonist
i. Run
at 0.5 - 5 mg/min
c. Permanent
pacemaker
i. Temporary
external pacer
d. If
due to surgical stimulation
i. Have
surgeon stop temporarily
ii. Give
atropine for bradycardia
vi. BUNDLE
BRANCH BLOCK
1. Characteristics-
a. Widened
QRS
b. PR
interval will be normal
2. With
BBB there is a delay in the depolarization of part of the ventricle by the
right or left bundle branches.
3. RIGHT
BBB
b. May
indicate a problem with the right side of the heart, but a RBBB with normal
axis and QRS duration may be normal.
d. QRS
duration 0.12s or greater.
e. Prominent
S wave in the lateral leads.
5. LEFT
BBB
a. LBBB-
This often indicates heart disease.
f. SICK
SINUS SYNDROME
i. Classified
as Bradycardia with episodes of SVT.
ii. Can
be due to degenerative changes of the SA node.
iii. Cardiac
pacemaker may be required if the drug therapy used to treat the tachycardiac
produces bradycardia.
iv. Drugs
used that may decrease heart rate are:
1. Digoxin,
calcium channel blockers, and Beta blockers.
v. ANESTHETIC
CONSIDERATIONS
1. These
patients may be on an anticoagulant.
2. May
require a temporary pacemaker if Bradycardia occurs.
3. Evaluation
of EKG.
4. Preop
assessment of symptoms:
a. Syncope,
dizziness, or patients may be asymptomatic.
g. PREMATURE
VENTRICULAR BEATS
ii. Lidocaine-
1-2mg/kg
iii. Treat
the underlying cause:
1. Hypoxemia
2. Hypercarbia
3. Hypokalemia
4. MI
h. VENTRICULAR
TACHYCARDIA
i. Is
identified as PVC’s > 3 in a row.
ii. The
QRS is wide- > 0.12 sec
iii. HR
> 120
iv. Asymptomatic
VT
1. Lidocaine-
1-2mg/kg
2. Procainamide-
Slows cardiac conduction impulses (blocks the rapid influx of sodium during
phase O depolarization)1.5mg/kg over one minute and repeat every 5 min (15mg/kg
max).
v. Symptomatic VT
1. External
defibrillation
i.
PROLONGED
QT INTERVAL
j.
i. QTc
> 0.44s
ii. Associated
with ventricular dysrrhythmias and sudden death.
iii. Treatment
1. Avoid
increasing SNS activity
2. Beta
blockers (esmolol)
iv. Seen
in : Patients with a congenital imbalance of the autonomic innervation to the
heart.
v. The
patient may require cardioversion.
k. WOLF-PARKINSON
WHITE SYNDROME
i. Caused
from an abnormal accessory pathway through the bundles
of kent [WU37] from the atria to the ventricle.
ii. The
AV node serves as the gait keeper electrical impulses from the SA node. If the
SA fires at an increased rate (ie Afib), the AV node will block half those
impulses.
iii. The
AV is also responsible for slowing of conduction.
iv. With
WPW atrial impulse will travel through the AV node and directly to the
ventricles.
v. The
rate of conduction through the accessory pathway is significantly increased.
vi. Cardiac
arrhythmias in addition to increased ventricular rate may lead to cardiac
arrest.
vii.
EKG
2. A
short PR interval
3. Wide
QRS
4. May
see T wave changes
viii. TREATMENT
1. May
depend on the type of re-entry tachyarrhythmia.
a. Orthodromic
AVRT-
i. Narrow complex QRS
ii. The
electrical signal travels through the AV node and then retrograde[WU39] back to the atria, exciting the atria at a
rapid rate.
b.
Antidromic
AVRT-
i. Wide
complex tachycardia
ix. ORTHODROMIC
AVRT
1. Treat
with carotid massage if asymptomatic, or valsalva maneuver.
2. Adenosine
6-12mg IV
3. If
unsuccessful, verapamil can be given or beta blockers
x. ANTIDROMIC
AVRT
1. Treatment
is intended on blocking the conduction pathway.
2. Verapamil
is not indicated here because of its inability to block cardiac conduction
along the accessory pathway, and also increase hypotension.
3. Digoxin
is also not indicated for the same reasons.
4. May
give procainamide if systolic bp is > 90
a. 10mg/kg
IV
b. Rate
max 50mg/min
5. Cardioversion
xi. SPECIAL
CONSIDERATIONS FOR AFIB AND WPW
1. Treatment
a. Procainamide
b. Verapamil
and Digoxin are contraindicated
i. These
drugs block conduction through the AV node and will enhance conduction through
the accessory pathway.
c. Cardiovesion-
if hemodynamically unstable.
xii. ANESTHETIC
MANAGEMENT
1. Aimed
at decreasing sns activity.
2. Give
sedative to reduce anxiety.
3. Glyco
and scopalamine preop is ok.
4. Have
drugs to treat tachyarrhythmias available.
5. Have
cardioversion available.
6. Avoid
the use of ketamine.
7. Give
NMB to facilitate intubation.
20. ARTIFICIAL
PACEMAKERS
a. Considerations:
i. preop-know
the types of pacemaker
ii. Rate
that it’s set.
iii. s/s.
Any dizziness or syncope in the past with the pacemaker.
iv. A
heart rate lower than the preset( by 10%) rate= battery malfunction.
v. Rate
of atrial/ventricular pacing indicates good generator function.
vi. An
irregular heart beat= pulse generator malfunction.
b. ANESTHETIC
MANAGEMENT
i. Use
of anesthetic drugs are not influenced by an artificial pacemaker.
ii. Have
atropine or isoproteronol ready in the event of failure or systole.
iii. Have
grounding pad for cautery placed as far from the generator as possible.
iv. Have
external converter magnet in the room (converts pacer from synchronized to a
synchronized mode).
[WU1]Halothane,
enflurane and iso depress SA node automaticity; only modest direct effects on
AV node, prolonged conduction time and incr refractoriness
VAAs decr heart contractility by decr entry of Ca2+
into cells (T&L Ca2+ channels) and decrease sensitivity of contractile
proteins to Ca2+
[WU4]Invasive
= cardiac cath; airline pilots need cardiac cath
Female > 45 y/o and male > 40 y/o needs preop EKG
[WU14]Induction,
intubation, emergence, surgical stimulation
Can give esmolol preop (b-blocker)
Try to minimize ischemia esp during induction or can
become extremely hypotensive – may give phenylephrine, etomidate, narcotic
induction (50-150 mcg/kg)
HTN pts have higher swings in BP; give lower doses
initially
[WU20]Hypotension
is usually volume related
**TACHYCARDIA has the largest effect on myocardial O2
demand
[WU21]Low
EF; VAA can cause myocardial depression
Sufentanyl or remifentanyl gtt with nitrous
Do not use pancuronium or succs; can incr HR
[WU35]L
BBB that developed intraop requires cardiac evaluation postop. Do not place PAC into patient with existing L
BBB à
PAC can cause R BBB which will cause complete HB
[WU44]Cautery
can interfere with pacemaker
Defibrillator needs to be deactivated
Need external defib during case
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